Reversible Sideroblastic Anemia Caused by Pyrazinoic Acid (Pyrazinamide®)

Case Studies1 June 1966Reversible Sideroblastic Anemia Caused by Pyrazinoic Acid (Pyrazinamide®)PAUL R. MCCURDY, M.D., F.A.C.P., ROBERT F. DONOHOE, M.D., MALCOLM MAGOVERN, M.D.PAUL R. MCCURDY, M.D., F.A.C.P.Search for more papers by this author, ROBERT F. DONOHOE, M.D.Search for more papers by this author, MALCOLM MAGOVERN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-64-6-1280 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptPyrazinoic acid amide*was introduced in 1952 for the treatment of tuberculosis. It was soon found to have significant hepatic toxicity and to produce an increase of serum uric acid which occasionally resulted in acute gouty arthritis. Since it offered no advantage over available compounds for the therapy of most patients with tuberculosis, it was relegated to use for patients with disease resistant to other antituberculosis drugs (1). Early reports contained no evidence for hematologic toxicity. More recently instances of sideroblastic anemia have been found during treatment with the antituberculosis drugs, cycloserine and pyrazinoic acid amide (2). This paper reports...References1. WOLINSKY E: Modern drug treatment of mycobacterial diseases. Med. Clin. N. Amer. 47: 1271, 1963. CrossrefMedlineGoogle Scholar2. VERWILGHENREYBROUCKCALLENSCOSEMANS RGLJ: Antituberculous drugs and sideroblastic anaemia. Brit. J. Haemat. 11: 92, 1965. CrossrefMedlineGoogle Scholar3. KIRKMANMCCURDYNAIMAN HNPRJL: Functionally abnormal glucose-6-phosphate dehydrogenases, in Cold Spring Harbor Symposia on Quantitative Biology, vol. XIX. Cold Spring Harbor Laboratory of Quantitative Biology, New York, 1964, p. 391. CrossrefGoogle Scholar4. 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Google Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAffiliations: Washington, D. C.From the Department of Medicine, Georgetown University School of Medicine and the Georgetown Medical Division and Pulmonary Disease Department, the District of Columbia General Hospital, Washington, D. C.This investigation was supported in part by grants AM 02823 and AM 09307 from the National Institute of Arthritis and Metabolic Diseases, National Institutes of Health, Bethesda, Md.Requests for reprints should be addressed to Paul R. McCurdy, M.D., D. C. General Hospital, 19th and E Streets, S. E., Washington, D. C. 20003.*Pyrazinamide®, Merck Sharp & Dohme, West Point, Pa. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDrug-induced red cell dyscrasiasPyrazinamide induced thrombocytopeniaA review of blood dyscrasias induced by the antituberculosis drugsErythropoeseRefractory Hypochromic AnemiasDrug-induced Mitochondrial Damage and Sideroblastic ChangeTuberculosis and the blood — A special relationship?Sideroblastic and Megaloblastic AnaemiasThrombocytopenia and Sideroblastic Anemia with Pyrazinoic Acid Amide (Pyrazinamide) TherapyPyridoxine- Responsive Anemias in ManReversible Megaloblastic and Sideroblastic Marrow Abnormalities in Alcoholic PatientsThe Effect of Riboflavin on Bone-Marrow Toxicity from Chloramphenicol 1 June 1966Volume 64, Issue 6Page: 1280-1284KeywordsAnemiaArthritisFolic acidHospital medicineIsoniazidMetabolic disordersPulmonary diseasesToxicityTuberculosisUric acid Issue Published: 1 June 1966 PDF downloadLoading ...